title: Detection of rupture-prone atherosclerotic plaques by time-resolved laser-induced fluorescence spectroscopy.
abstract: OBJECTIVE
  Plaque with dense inflammatory cells, including macrophages, thin fibrous cap and superficial necrotic/lipid core is thought to be prone-to-rupture. We report a time-resolved laser-induced fluorescence spectroscopy (TR-LIFS) technique for detection of such markers of plaque vulnerability in human plaques.
  
  
  METHODS
  The autofluorescence of carotid plaques (65 endarterectomy patients) induced by a pulsed laser (337 nm, 0.7 ns) was measured from 831 distinct areas. The emission was resolved spectrally (360-550 nm range) and temporally (0.3 ns resolution) using a prototype fiber-optic TR-LIFS apparatus. Lesions were evaluated microscopically and quantified as to the % of different components (fibrous cap, necrotic core, inflammatory cells, foam cells, mature and degraded collagen, elastic fibers, calcification, and smooth muscle cell of the vessel wall).
  
  
  RESULTS
  We determined that the spectral intensities and time-dependent parameters at discrete emission wavelengths (1) allow for discrimination (sensitivity >81%, specificity >94%) of various compositional and pathological features associated with plaque vulnerability including infiltration of macrophages into intima and necrotic/lipid core under a thin fibrous cap, and (2) show a linear correlation with plaque biochemical content: elastin (P<0.008), collagen (P<0.02), inflammatory cells (P<0.003), necrosis (P<0.004).
  
  
  CONCLUSIONS
  Our results demonstrate the feasibility of TR-LIFS as a method for the identification of markers of plaque vulnerability. Current findings enable future development of TR-LIFS-based clinical devices for rapid investigation of atherosclerotic plaques and detection of those at high-risk.
authors.affiliation: University of California Davis, Department of Biomedical Engineering, Davis, CA 95616, USA. lmarcu@ucdavis.edu
authors.forename: Laura
authors.initials: L
authors.lastname: Marcu
authors.forename: Javier A
authors.initials: JA
authors.lastname: Jo
authors.forename: Qiyin
authors.initials: Q
authors.lastname: Fang
authors.forename: Thanassis
authors.initials: T
authors.lastname: Papaioannou
authors.forename: Todd
authors.initials: T
authors.lastname: Reil
authors.forename: Jian-Hua
authors.initials: JH
authors.lastname: Qiao
authors.forename: J Dennis
authors.initials: JD
authors.lastname: Baker
authors.forename: Julie A
authors.initials: JA
authors.lastname: Freischlag
authors.forename: Michael C
authors.initials: MC
authors.lastname: Fishbein
mesh_terms: D002114:Calcinosis / Q000473:pathology; D002340:Carotid Artery Diseases / Q000378:metabolism / Q000473:pathology* / Q000601:surgery; D017536:Carotid Artery, Common / Q000737:chemistry / Q000473:pathology* / Q000601:surgery; D003094:Collagen / Q000032:analysis; D004549:Elastin / Q000032:analysis; D016894:Endarterectomy, Carotid; D005240:Feasibility Studies; D005336:Fiber Optic Technology; D005355:Fibrosis; D005487:Foam Cells / Q000473:pathology; D006801:Humans; D007834:Lasers; D008055:Lipids / Q000032:analysis; D009336:Necrosis; D011237:Predictive Value of Tests; D015203:Reproducibility of Results; D012421:Rupture; D012680:Sensitivity and Specificity; D013050:Spectrometry, Fluorescence / Q000379:methods*; D013997:Time Factors
chemical_list: D008055:Lipids; D003094:Collagen; D004549:Elastin